Unexpected function of dyslexia gene

June 20, 2011

(Medical Xpress) -- Scientists at Karolinska Institutet have discovered that a gene linked to dyslexia has a surprising biological function: it controls cilia, the antenna-like projections that cells use to communicate.

Dyslexia is largely hereditary and linked to a number of genes, the functions of which are, however, largely unknown. This present study from Karolinska Institutet and Helsinki University now shows that one of these genes, DCDC2, is involved in regulating the signalling of cilia in .

"Our discovery presents us with a possible new neurobiological mechanism for dyslexia," says Professor Juha Kere, who co-led the study with Professor Eero Castr?n of Helsinki University.

Cilia are hair-like structures that project from the surface of most cells. Their purpose has long remained something of a mystery, but recent research has revealed that the cells use them to communicate and that they play a crucial part in the development of the body's organs.

These results tie into previous research in mice showing that DCDC2 and two other dyslexia genes are involved in cell migration, a process by which nerve cells are moved to their correct location in the brain during embryonic development.

"The cilia are important parts of the machinery that controls ," says Professor Kere. "Just what they do and how it could result in dyslexia are interesting questions that will be given further study."

The new findings, which are presented in the scientific journal PLoS ONE show that DCDC2 governs the length of the cilia and activates two different signal systems in the cell, depending on the degree of . When the human variant of the gene was transferred to in the roundworm C. elegans, it gave rise to unusual neural projections exclusively in ciliated cells.

Ciliary dysfunction in different organs has been associated with a wide range of disorders from rare genetic diseases such as polycystic and Kartagener's syndrome, to diabetes, obesity and schizophrenia.

Explore further: Scientists study cilia -- microscopic hair

More information: Satu Massinen, Marie-Estelle Hokkanen, Hans Matsson, Kristiina Tammimies, Isabel Tapia-Paez, Vanina Dahlström-Heuser, Juha Kuja-Panula, Jan Burghoorn, Kristian E. Jeppsson, Peter Swoboda, Myriam Peyrard-Janvid, Rune Toftgard, Eero Castrén, Juha Kere, Increased expression of the dyslexia candidate gene DCDC2 affects length and signaling of primary cilia in neurons, PLoS ONE 16 June 2011; 6(6): e20580.doi:10.1371/journal.pone.0020580

Related Stories

Scientists study cilia -- microscopic hair

May 5, 2006

Texas scientists studying microscopic hairs called cilia say they found an internal structure that's responsible for a cell's response to external signals.

German scientists find dyslexia gene

June 20, 2006

German researchers say they've found a genetic component for the learning disability dyslexia, possibly opening new methods of treatment.

Researchers identify new role for cilia protein in mitosis

April 4, 2011

Researchers at the University of Massachusetts Medical School have described a previously unknown role for the cilia protein IFT88 in mitosis, the process by which a dividing cell separates its chromosomes containing the ...

How cells' sensing hairs are made

June 8, 2011

(PhysOrg.com) -- Body cells detect signals that control their behavior through tiny hairs on the cell surface called cilia. Serious diseases and disorders can result when these cilia do not work properly. New research from ...

Recommended for you

Researchers discover otulipenia, a new inflammatory disease

August 22, 2016

National Institutes of Health researchers have discovered a rare and sometimes lethal inflammatory disease - otulipenia - that primarily affects young children. They have also identified anti-inflammatory treatments that ...

Solving the mystery of meningiomas reveals a surprise twist

August 23, 2016

In solving one mystery—the genetic roots of benign brain tumors called meningiomas—a team of scientists led by Yale researchers stumbled upon an even greater one: How is it possible that two of the mutations linked to ...

0 comments

Please sign in to add a comment. Registration is free, and takes less than a minute. Read more

Click here to reset your password.
Sign in to get notified via email when new comments are made.